This study aims to determine how much non-random V gene usage there is at the level of V(D)J rearrangement, what factors influence non-equal gene rearrangement, how much initial junctional diversity is created and how much is selection acting upon the initial rearrangement, and to test the hypothesis that the anti-Hib response is slow to arise in ontogeny because the VkA2 gene will rearrange very infrequently due to its distal inverted location. Further, we will test the hypothesis that resistance to a bacteria which infects infants would be primarily due to germline genes which can encode antibodies with sufficient affinity for the antigen.